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Scientists may have found a way to stop Alzheimer’s damage before it starts — by “melting” the tiny protein clumps that are the early triggers of the disease.
Alzheimer’s has long been linked to harmful tau protein fibrils that build up in the brain and interfere with cognitive function, but researchers have now discovered soft, small clusters that appear first.
When those early clusters were dissolved, it prevented the toxic fibrils from forming, which could effectively block the disease, according to researchers from Tokyo Metropolitan University.
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Led by Professor Rei Kurita, the scientists used precise X-ray and fluorescence methods in a laboratory setting to find the microscopic “precursors,” which measured only tens of nanometers, according to a press release.
Because the tiny precursors were soft, the researchers were able to dissolve them. As a result, no tau fibrils were formed.
These results suggest a shift in how scientists might develop Alzheimer’s disease treatments.
Rather than focusing on breaking apart the final fibril formations, new therapies could target the earlier, reversible precursor stage to prevent harmful structures from forming in the first place, according to the release.
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This strategy could eventually be applied to the research of neurodegenerative diseases like Parkinson’s.
The study did have some limitations, primarily that it involved in-vitro biochemical models and no humans or animals. It’s not known whether similar reversible clusters exist in human brain tissue.
More research is needed to find out if breaking up these protein clusters is safe and could actually help treat the disease.
Dr. Marc Siegel, Fox News senior medical analyst, was not involved in the study but shared his reactions to the findings.
“There are three essential components structurally involved in the development of Alzheimer’s disease — beta amyloid proteins, tau proteins and neuroinflammation,” he told Fox News Digital.
“In the future, there will likely be triple therapy — anti-inflammation, anti-beta-amyloid and anti-tau.”
“There are already treatments on the market to target beta amyloid buildup, and now here’s a targeted therapy to dissolve and disrupt tau protein buildup before it forms the dreaded neurofibrillatory tangles.”
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Siegel believes this is “bound to be of clinical value” and will likely be better tolerated than other medications currently on the market.
“In the future, there will likely be triple therapy — anti-inflammation, anti-beta-amyloid and anti-tau,” he predicts.
Courtney Kloske, Ph.D., director of scientific engagement for the Alzheimer’s Association in Chicago, also reacted to the study in an interview with Fox News Digital.
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“This manuscript focuses on altering the structure of tau, one of the hallmark brain proteins involved in Alzheimer’s, and on exploring approaches that could potentially slow or stop disease development,” said Kloske, who was also not involved in the study.
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“This is promising basic research that may turn out to deepen our understanding of the mechanisms underlying the disease, but it is preliminary, and additional studies are needed to determine how these findings can be translated into human studies.”
Fox News Digital reached out to the researchers for comment.
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